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Intercoronary collaterals without obstructive coronary artery disease
942
LETTERS
rudimentary left ventricle. No examples of the latter group are included in the Mayo Clinic study. This may be because they have not seen or recognized any. However, this is unlikely since fair-sized series have been accumulated from centers dealing with a similar work load. 3,4 It is more likely that cases were excluded because there is no consensus as to whether they are "univentricular. ''1,5 It is important to know if this is the case, because ventricular morphology could well be a significant determinant of long-term survival. I submit that cases with double inlet right ventricle and rudimentary left ventricle are appropriately grouped with the Mayo Clinic material because all have a double or common inlet atrioventricular connection. Furthermore, recognition of this fact resolves the controversy concerning "univentricular hearts" and the "single ventricle trap. ''2 Robert H. Anderson, MD London, England 1. Anderson RH, Tynan MJ, Freedom RM el al. VenVicular morphology in the univentricular heart. Herz 1979;4: 184-197. 2. Anderson RH, Macertney FJ, Tynee M el el. Univantricular atrioventricular connection: the single ventricle trap unsprung. Pod Cardio11983;4:273-280. 3. Keelon BR, Macedsey FJ, Hunter S el el. Univentrlcular heart of right ventrlcular type with double or common inlet. Circulation 1979;59:403-411. 4. Selo B, Bedranee EG, BeeemPR, Seeza A ,k, Bargeron LM Jr. Angiograghic study of unlventricularheart of right ventricular type. Circulation 1979;60:1325-1334. 5. Van Praagh R, David I, Van Praagh S. What is a ventricle? The single ventricle trap. Pod Cardlol 1982;2: 79-84.
M E C H A N I S M FOR IMPROVED H E M O D Y N A M I C S WITH DUALC H A M B E R PACING IN PATIENTS WITH CAROTID SINUS HYPERSENSITIVITY
Madigan et al 1 have done an interesting study of the hemodynamic effects of ventricular vs dual-chamber pacing in patients with carotid sinus hypersensitivity, but the study design does not provide sufficient evidence to support the prol~osed mechanism for the different responses. The authors hypothesize that the significantly worsened hemodynamics observed during carotid sinus massage with VVI pacing are secondary to an "aggravation of the vasodepressor component." They did not, however, assess the hemodynamic effect of ventricular pacing in the absence of carotid sinus massage (the pacemaker effect2-4). The degree of hypotension associated with ventricular pacing in the basal state must be determined before one can assess the relative contribution of vasodepressor hypersensitivity to hypotension occurring with carotid
sinus massage during VVI pacing. This can be accomplished by following hemodynamics while increasing the pacemaker rate (while in VVI mode) from one less than that of sinus to one sufficient to overdrive the sinus rhythin, s Morley et al 5 studied patients who remained symptomatic after a VVI pacemaker was placed for treatment of symptomatic cardioinhibitory hypersensitivity, and assessed the relative contribution of concomitant vasodepressor hypersensitivity and pacemaker effect toward the continued symptoms. The majority of these patients had symptoms secondary to a combination of pacemaker effect and vasodepressor hypersensitivity, neither of which was independently strong enough to cause symptoms. Morley postulated that these patients would benefit from elimination of the pacemaker effect with dual-chamber pacing, and was successful in relieving symptoms in a large percentage. There was much less success among patients who were symptomatic on the basis solely of a strong vasodepressor response. It is possible that the elimination of a pacemaker effect, rather than a direct effect on vasodepressor hypersensitivity, is the mechanism for improved hemodynamics with dual-chamber pacing in Madigan's study also. Nell L. Coplan, MD New York, New York 1. Madlgan NP, Flaker GC, Curtis JJ, Reid J, Mueller J, MurphyTJ. Carotid sinus hypersensitivity: beneficial effects of dual chamber pacing. Am J Cardiol 1984; 53:1034-1040. 2. Haas JM, Stra# GB. Pacamaker-lnducedcardlovescula~ failure: bemodycamic and anglographic observations. Am J Cardlol 1974;33:295-299. 3. AIIcandrl C, Fouad FM, Tarazl RC, Castle L, Morant V. Three cases of hypotacsion and syncope with vefltrlcular pacing: possible role of al;'lal reflexes. Am J Cerdlol 1978;42:137-142. 4. Gamol M, Van Geldor LM. Chronic ventrlcuiar pacing with ventrlculo-atrlal conduction versus atrial pacing in three patients wl~ symptomatic sinus bredycardla.PACE 1981;4:100-105. 5. Morley CA, Perdne EJ, Grant P, Chart SL, McBrkm DJ, Suflon R. Carotid sinus syncope treated by pacing, Br Heart J 1982;47:411-418.
AJMALINE
CARDIOTOXICITY
In their recent report on nonfatal ajmaline cardiotoxicity in 2 patients with Chagasic cardiomyopathy, Medina-Ravell et al I concluded that "further studies are required to evaluate if toxicity with relatively small doses of ajmaline occurs in patients with organic heart disease of other causes." Although major complications of the ajmaline test are rare, 2-4 they almost always occur in patients with organic heart disease. 2~ In addition, cardiomegaly associated with heart failure
(even compensated) as present in the 2 casea of this report are considered by most inves~ tigators as definite contraindications of the ajmaline test. 2,4 Therefore, we believe tha~ prospective studies of the ajmaline test ir~ patients with organic heart disease should ~ carefully take into account the contraindications of this test in order to minimize the incidence of major complications. Bernard Belhasoen, MD Philadelphia,Pennsylvania Gilbert Moltb, MD Clamart, France 1. Medlna-Ravoll V, Rodrlguez-Salse L, Mendoza IJ, Caelellance A. Nonfatal aJmallne cardiotoxiclty. Am J Cardiol 1984;53:958-959. 2. Motl6 G, Belhassen B, Vogel M, Belianger P, Weltl JJ. Etude critique des explorations endocavltaires dens le diagnostic des blocs aurlculoventriculaires paroxystiquas. Ann Cardlol Angalol 1975;24:557-568. 3. Perrot B, Allot E, GIIgenkrantz JM, Chortler F, Folvre G. Exploration endocavitaire hisienne. Apperts du test ~, I'ajmallne. Rev Port Cardlol 1982;2:285-294. 4. Caromella JP, Gu~rel C, Valbre PE, Tricot R, Bismuth C, Rib(inlet G. Toxlcit0 cardiaqce d I'aJmallne. Comparalson des Intoxications algues volontalres el des accidents du test & I'ajmallne. Arch Mal Coeur 1982; 75:613-620. 5. Wellens HJJ, Rat FW, Vanagi EJ. Death after aJmallne administration (latter to the editor). Am J Cerdiol 1980;45:905.
INTERCORONARY COLLATERALS W I T H O U T OBSTRUCTIVE C O R O N A R Y A R T E R Y DISEASE I read with interest the recent case report by Linsenmeyer and SchneideP of angiographic demonstration of intercoronary collaterals in the absence of obstructive coronary artery disease. The authors cited 1 other case report 2 of collaterals from right coronary artery to circumflex artery in the absence of disease in the latter vessel. I reported the first arteriographic demonstration of collateral circulation from the right coronary artery to the left anterior descending artery in a man without coronary artery disease. 3 With the large number of coronary arteriograms performed now, some of which were apparently on persons with normal coronary arteries, I wonder why there are not more such case reports. Tsung O. Cheng, MD Washington, D.C. 1. Llesenmeyor GJ M, Schneider JF. Angiographlcelly visible intercorcoary collateral circulation in the absence of obstructive coronary artery disease. Am J Cardiol 1984;53:954-956. 2. Welner BH, Mills RM, Starobln O, Ungley JF. Intracorocary anastomosis in the absence of obstructive lesions of the coronary arteries. Chest 1979;76:488-489. 3. ChangTO. ArtorloITaphicdemoestrationof Intercorcoary arterial anastomosis in a living man without coronary artery disease. Anglology 1972;23:76-88.
LETTERS
rudimentary left ventricle. No examples of the latter group are included in the Mayo Clinic study. This may be because they have not seen or recognized any. However, this is unlikely since fair-sized series have been accumulated from centers dealing with a similar work load. 3,4 It is more likely that cases were excluded because there is no consensus as to whether they are "univentricular. ''1,5 It is important to know if this is the case, because ventricular morphology could well be a significant determinant of long-term survival. I submit that cases with double inlet right ventricle and rudimentary left ventricle are appropriately grouped with the Mayo Clinic material because all have a double or common inlet atrioventricular connection. Furthermore, recognition of this fact resolves the controversy concerning "univentricular hearts" and the "single ventricle trap. ''2 Robert H. Anderson, MD London, England 1. Anderson RH, Tynan MJ, Freedom RM el al. VenVicular morphology in the univentricular heart. Herz 1979;4: 184-197. 2. Anderson RH, Macertney FJ, Tynee M el el. Univantricular atrioventricular connection: the single ventricle trap unsprung. Pod Cardio11983;4:273-280. 3. Keelon BR, Macedsey FJ, Hunter S el el. Univentrlcular heart of right ventrlcular type with double or common inlet. Circulation 1979;59:403-411. 4. Selo B, Bedranee EG, BeeemPR, Seeza A ,k, Bargeron LM Jr. Angiograghic study of unlventricularheart of right ventricular type. Circulation 1979;60:1325-1334. 5. Van Praagh R, David I, Van Praagh S. What is a ventricle? The single ventricle trap. Pod Cardlol 1982;2: 79-84.
M E C H A N I S M FOR IMPROVED H E M O D Y N A M I C S WITH DUALC H A M B E R PACING IN PATIENTS WITH CAROTID SINUS HYPERSENSITIVITY
Madigan et al 1 have done an interesting study of the hemodynamic effects of ventricular vs dual-chamber pacing in patients with carotid sinus hypersensitivity, but the study design does not provide sufficient evidence to support the prol~osed mechanism for the different responses. The authors hypothesize that the significantly worsened hemodynamics observed during carotid sinus massage with VVI pacing are secondary to an "aggravation of the vasodepressor component." They did not, however, assess the hemodynamic effect of ventricular pacing in the absence of carotid sinus massage (the pacemaker effect2-4). The degree of hypotension associated with ventricular pacing in the basal state must be determined before one can assess the relative contribution of vasodepressor hypersensitivity to hypotension occurring with carotid
sinus massage during VVI pacing. This can be accomplished by following hemodynamics while increasing the pacemaker rate (while in VVI mode) from one less than that of sinus to one sufficient to overdrive the sinus rhythin, s Morley et al 5 studied patients who remained symptomatic after a VVI pacemaker was placed for treatment of symptomatic cardioinhibitory hypersensitivity, and assessed the relative contribution of concomitant vasodepressor hypersensitivity and pacemaker effect toward the continued symptoms. The majority of these patients had symptoms secondary to a combination of pacemaker effect and vasodepressor hypersensitivity, neither of which was independently strong enough to cause symptoms. Morley postulated that these patients would benefit from elimination of the pacemaker effect with dual-chamber pacing, and was successful in relieving symptoms in a large percentage. There was much less success among patients who were symptomatic on the basis solely of a strong vasodepressor response. It is possible that the elimination of a pacemaker effect, rather than a direct effect on vasodepressor hypersensitivity, is the mechanism for improved hemodynamics with dual-chamber pacing in Madigan's study also. Nell L. Coplan, MD New York, New York 1. Madlgan NP, Flaker GC, Curtis JJ, Reid J, Mueller J, MurphyTJ. Carotid sinus hypersensitivity: beneficial effects of dual chamber pacing. Am J Cardiol 1984; 53:1034-1040. 2. Haas JM, Stra# GB. Pacamaker-lnducedcardlovescula~ failure: bemodycamic and anglographic observations. Am J Cardlol 1974;33:295-299. 3. AIIcandrl C, Fouad FM, Tarazl RC, Castle L, Morant V. Three cases of hypotacsion and syncope with vefltrlcular pacing: possible role of al;'lal reflexes. Am J Cerdlol 1978;42:137-142. 4. Gamol M, Van Geldor LM. Chronic ventrlcuiar pacing with ventrlculo-atrlal conduction versus atrial pacing in three patients wl~ symptomatic sinus bredycardla.PACE 1981;4:100-105. 5. Morley CA, Perdne EJ, Grant P, Chart SL, McBrkm DJ, Suflon R. Carotid sinus syncope treated by pacing, Br Heart J 1982;47:411-418.
AJMALINE
CARDIOTOXICITY
In their recent report on nonfatal ajmaline cardiotoxicity in 2 patients with Chagasic cardiomyopathy, Medina-Ravell et al I concluded that "further studies are required to evaluate if toxicity with relatively small doses of ajmaline occurs in patients with organic heart disease of other causes." Although major complications of the ajmaline test are rare, 2-4 they almost always occur in patients with organic heart disease. 2~ In addition, cardiomegaly associated with heart failure
(even compensated) as present in the 2 casea of this report are considered by most inves~ tigators as definite contraindications of the ajmaline test. 2,4 Therefore, we believe tha~ prospective studies of the ajmaline test ir~ patients with organic heart disease should ~ carefully take into account the contraindications of this test in order to minimize the incidence of major complications. Bernard Belhasoen, MD Philadelphia,Pennsylvania Gilbert Moltb, MD Clamart, France 1. Medlna-Ravoll V, Rodrlguez-Salse L, Mendoza IJ, Caelellance A. Nonfatal aJmallne cardiotoxiclty. Am J Cardiol 1984;53:958-959. 2. Motl6 G, Belhassen B, Vogel M, Belianger P, Weltl JJ. Etude critique des explorations endocavltaires dens le diagnostic des blocs aurlculoventriculaires paroxystiquas. Ann Cardlol Angalol 1975;24:557-568. 3. Perrot B, Allot E, GIIgenkrantz JM, Chortler F, Folvre G. Exploration endocavitaire hisienne. Apperts du test ~, I'ajmallne. Rev Port Cardlol 1982;2:285-294. 4. Caromella JP, Gu~rel C, Valbre PE, Tricot R, Bismuth C, Rib(inlet G. Toxlcit0 cardiaqce d I'aJmallne. Comparalson des Intoxications algues volontalres el des accidents du test & I'ajmallne. Arch Mal Coeur 1982; 75:613-620. 5. Wellens HJJ, Rat FW, Vanagi EJ. Death after aJmallne administration (latter to the editor). Am J Cerdiol 1980;45:905.
INTERCORONARY COLLATERALS W I T H O U T OBSTRUCTIVE C O R O N A R Y A R T E R Y DISEASE I read with interest the recent case report by Linsenmeyer and SchneideP of angiographic demonstration of intercoronary collaterals in the absence of obstructive coronary artery disease. The authors cited 1 other case report 2 of collaterals from right coronary artery to circumflex artery in the absence of disease in the latter vessel. I reported the first arteriographic demonstration of collateral circulation from the right coronary artery to the left anterior descending artery in a man without coronary artery disease. 3 With the large number of coronary arteriograms performed now, some of which were apparently on persons with normal coronary arteries, I wonder why there are not more such case reports. Tsung O. Cheng, MD Washington, D.C. 1. Llesenmeyor GJ M, Schneider JF. Angiographlcelly visible intercorcoary collateral circulation in the absence of obstructive coronary artery disease. Am J Cardiol 1984;53:954-956. 2. Welner BH, Mills RM, Starobln O, Ungley JF. Intracorocary anastomosis in the absence of obstructive lesions of the coronary arteries. Chest 1979;76:488-489. 3. ChangTO. ArtorloITaphicdemoestrationof Intercorcoary arterial anastomosis in a living man without coronary artery disease. Anglology 1972;23:76-88.